Surgical Procedures/Acid Base Disorder

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Acid Base Disorder

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In general : H+ = 24 × PCO2/HCO3–
(Usually in clinical practice, H+ concentration is expressed as pH.)

  • Normal pH = 7.35–7.45.
    • Acidemia = pH < 7.35.
    • Alkalemia = pH > 7.45.
  • PaCO2 (Arterial CO2 concentration normal = 35–45 mm Hg).
  • HCO3– (Serum electrolytes normal = 22–31 mmol/liter).


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  • Acidosis is a process that causes the accumulation of acid.
  • Alkalosis is a process that causes the accumulation of alkali.

Respiratory Acidosis-Alkalosis

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Disorders that initially alter arterial PCO2 (arterial CO2 concentration) are termed respiratory acidosis-alkalosis.

Metabolic Acidosis-Alkalosis

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Disorders initially affecting HCO3– (serum electrolytes) concentration are termed metabolic acidosis-alkalosis.

Metabolic Alkalosis

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  1. Chloride-responsive.
    • The most common causes in the surgical practice include:
      • Diuretic therapy (e.g., contraction alkalosis).
      • Acid loss through GI secretions (e.g., nasogastric suctioning, vomiting).
      • Exogenous administration of HCO3– or HCO3– precursors (e.g., citrate in blood).
  2. Chloride-unresponsive metabolic alkalosis is comparatively less common and includes:
    • Hyperaldosteronism
    • Marked hypokalemia
    • Renal failure
    • Renal tubular Cl– wasting (Bartter’s syndrome)
    • Oedematous states.
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Measurement of urinary chloride concentration.

  • Suggestive causes of the metabolic alkalosis if Urine Cl– concentration is <15 mmol/liter:
    • vomiting.
    • nasogastric suctioning.
    • postdiuretic administration.
    • posthypercapnia.
  • Sughgestive causes of the metabolic alkalosis if Urine Cl– concentration is > 20 mmol/liter:
    • Mineralocorticoid excess.
    • Alkali loading.
    • Concurrent diuretic administration
    • Presence of severe hypokalemia.
Treatment principles in metabolic alkalosis:
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Goal of Treatments can be:

  1. Removing and identifying underlying causes, Discontinuing exogenous alkali, repairing Cl–, K+, and volume deficits.
  2. Correction of volume deficits (can be used 0.9% NaCl) and hypokalemia.
  3. H2-receptor antagonists or other acid-suppressing medications can be used after vomiting or nasogastric suctioning.
  4. If Edemea:
    • Acetazolamide (5 mg/kg/day IV or PO) can be used.
      • Eases fluid mobilization while decreasing renal HCO3– reabsorption.
      • Tolerance to this diuretic may develop after 2–3 days.
  5. Ammonium chloride (NH4Cl) can be used in severe alkalemia (HCO3– >40 mmol/liter; rate not exceeding 5 ml/minute).
    • Approximately one-half of the calculated volume of NH4Cl is usually administered and the acid-base status and Cl– concentration is usually rechecked to determine the need of further treatment.
    • Hepatic failure is contraindication for NH4Cl.
  6. HCl more rapidly corrects metabolic alkalosis.
  7. Dialysis:
    • Can be considered in the volume-overloaded situation with renal failure and intractable metabolic alkalosis.
Estimation of the amount of H+ requirement
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The amount of H+ to administer may be estimated by the following equation:
H+(mmol) = 0.5 × wt (kg) × [103 – serum Cl– (mmol/liter)]

Estimation of the amount of NH4Cl requirement:
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Can be estimated by the following equation: NH4Cl (mmol) = 0.2 × wt (kg) × [103 – serum Cl– (mmol/liter)]

Metabolic Acidosis

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(Low pH with low CO2 content)

  • Reduction in plasma Bicarbonate and a consequence rise in H+.
  • PaCO2 is reduced secondarily by Hyperventilation, which mitigates the rise in H+.
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Metabolic Acidosis is caused if:

  • Accumulation of nonvolatile acids.
  • Reduction of renal acid excretion.
  • Loss of alkali.
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1. Methyl Alcohol. 2. Uremia. 3. Diabetic Ketoacidosis 4. Para-Aldehyde poisoning. 5. Ischemia. 6. Lactic acidosis. 7. Ethylene Glycol Alcohol ingestion. 8. Salicylic Poisoning.

Other commonest causes are:
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  • Addition of excessive acids to plasma.
    • Ketoacidosis, Lacticacidosis.
    • Methanol, ethylene glycol and salicylic poisoning.
  • Failure to excrete acid:
    • Chronic Renal Failure.
    • Acute Renal Failure etc
  • Loss of Bicarbonate (base):
    • From G.I.T:
      • Diarrhea.
      • Fistulae.
    • In Urine:
    • Proximal renal tubular acidosis.
    • Carbonic anhydrase inhibitors.
Clinical Feature
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  1. Usually in severe cases Kussmaul's respiration can be present.
  2. When H+ >70 mmol/L; then,
    • Cardiac-Out-Put falls.
    • Blood pressure decreases.
    • Frequnet confusion.
    • Drowsiness.
Diagnostic Classsification (Anion Gap)
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Anion gap (AG: normal, 3–11 mmol/liter)
AG (mmol/liter) = Na+ (mmol/liter) – [Cl– (mmol/liter) + HCO3– (mmol/liter)]

It is useful diagnostically to classify metabolic acidosis into:

  1. Increased AG metabolic acidosis.
  2. Normal AG metabolic acidosis.
Causes according to Anion Gap:
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Increased anion gap Metabolic Acidosis:
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  1. Increased acid production:
    1. Ketoacidosis
      1. Diabetic
      2. Alcoholic
      3. Starvation
    2. Lactic acidosis
    3. Toxic ingestion:
      1. Salicylates.
      2. Ethylene glycol.
      3. Methanol.
  2. Renal failure.
Normal anion gap (hyperchloremic) Metabolic Acidosis:
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  1. Renal tubular dysfunction
    1. Renal tubular acidosis.
    2. Hypoaldosteronism.
    3. Potassium-sparing diuretics.
  2. Loss of alkali.
    1. Diarrhea.
    2. Ureterosigmoidostomy.
    3. Carbonic anhydrase inhibitors.
  3. Administration of HCl (ammonium chloride, cationic amino acids).
Management/Treatment of metabolic acidosis:
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  • Directed primarily towards the underlying cause of the acid-base disturbance.
  • Bicarbonate therapy is considered when there is moderate to severe metabolic acidosis, depending on the etiology.
  1. Infusion of NaHCO3, stoped when H+ is normol.
  2. Monitoring H+ and HCO3-
  3. Treatment of underlying causes.

The HCO3– deficit (mmol/liter) can be estimated by the following equation:

HCO3– deficit (mmol/liter) = Body weight (kg) × 0.4 × [desired HCO3– (mmol/liter) – measured HCO3– (mmol/liter)]

(This equation serves only as a rough estimate .)

The goal of HCO3–
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  • To raise the arterial blood pH to 7.00 or the HDRO3– concentration to 10 mmol/liter.
    • Risks of bicarbonate therapy:
      • Hypernatremia.
      • Hypercapnia.
      • Cerebrospinal fluid acidosis.
      • Overshoot alkalosis.

Serial arterial blood gases and serum electrolytes should be obtained to assess the response to HCO3– therapy.

Rate of HCO3– replacement:
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  • In nonurgent situations:
    • Continuous intravenous infusion over 4–8 hours (50-ml ampule of 8.4% NaHCO3 solution provides 50 mmol of HCO3–) can be added to 1 liter of D5W or 0.45% NaCl.
  • In urgent situation:
    • Deficit can be administered as a bolus over several minutes.